Post-viral vagal neuropathy (PVVN) refers to a condition in which the distal branches of the vagus nerve malfunction following a viral infection. In the larynx, the vagus nerve supplies all of the intrinsic muscles for vocal cord movement, as well as sensation to the mucosal lining. Among the many thousands of cases of a paralyzed vocal cord that are diagnosed each year, about one-fourth have no clear cause (they are ?idiopathic?); these are widely believed to be caused by an upper respiratory system virus, since the onset of hoarseness from the paralyzed cord seems to occur during this infection in many cases. This constitutes the motor type of PVVN. Another group of patients has a severe chronic cough that is triggered by the smallest of stimuli; this is believed to be a sensory type of PVVN. Together, the motor and sensory types of PVVN affect thousands of patients each year, and both types can be quite debilitating. Despite this high incidence, there has been absolutely no research into the problem. This likely relates to a lack of an animal model to carry out such studies. This project seeks to develop an animal model so that PVVN can be studied and effective treatments can be found. In a rat model, selected viruses (from the same families as those commonly involved in human URIs) will be inoculated into the tissues of the larynx, simulating the presumed route by which the virus involves the nerve in humans. Two models will be studied. In the first model, the nerve branches targeted supply movement of the laryngeal muscles; a successful inoculation will result in a paralyzed vocal cord. The strength of the muscles will be measured as an indicator of partial paralysis (paresis), complete paralysis, or no paralysis. In the second model, the nerve targeted is the sensory nerve to the mucosal lining at the top of the larynx. A system of testing the sensation will be employed that delivers small puffs of air at various pressures, to see how sensitive the tissue is. The successful viral neuropathy model will begin by making the nerve numb, but later the nerve will recover to become hypersensitive. This would simulate the clinical experience of patients with PVVN. For both models, once a successful viral injection is found, a series of animals will be followed over time to see whether the neuropathy recovers. Mechanisms of injury and recovery will be studied using histologic evaluation of the larynx and nerves. Development of an animal model is the first step to finding an effective treatment for the difficult problem of PVVN.